Beth A. McCormick^1,2, Samuel I. Miller³, and James L. Madara^1,2.

¹ Departments of Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA 02115

² The Harvard Digestive Diseases Center

³ Departments of Medicine and Microbiology, University of Washington, Seattle, WA 98195.

Received 06/19/96; Accepted 07/09/96; On-line 08/01/96

5. PERSPECTIVE

In recent years some eminent advances have been made in the basic understanding of how Salmonella interact with intestinal epithelial cells, their host cell target. Specifically, this review examined the current insights on the molecular pathways utilized by Salmonella spp. in cell binding that are important for the promotion of Salmonella disease pathogenesis. The most progress has been made in the area of the molecular genetic basis of Salmonella entry into mammalian cells. However, there has recently been an emanation of information concerning the basic understanding of how Salmonella binding to epithelial cells coordinates the mucosal inflammatory response. Importantly, a common theme to emerge from such fertile areas of research is that upon Salmonella binding to epithelial cells, the host cell plays an active role in not only Salmonella internalization, but also in generating proinflammatory signals which lead to active states of intestinal inflammation. Of course, while many questions await answers, future investigations can only shed more light on the pathogenic mechanisms which govern Salmonella binding to epithelial cells.